The behavior of the 2006 ten Tusscher-Panfilov model of human ventricular myocytes under the impact of periodic excitation impulses was studied in the BeatBox simulation environment. The cardiomyocyte model has a limi...The behavior of the 2006 ten Tusscher-Panfilov model of human ventricular myocytes under the impact of periodic excitation impulses was studied in the BeatBox simulation environment. The cardiomyocyte model has a limited susceptibility to an forced higher frequency excitation rhythm. A high-frequency excitation rhythm can be forced by gradually increasing the frequency of excitation impulses. The mechanism of defibrillation pulse impact consists of presumably prolonging the refractoriness of cardiomyocytes which undermines their susceptibility for a long time to a forced high-frequency rhythm of fibrillation, as a result for which they hinder the propagation of a fibrillation wave. This is the only mechanism of defibrillation that was identified during the simulation. The threshold energy of a depolarizing defibrillation pulse prolonging the refractoriness of the cardio-myocyte varies depending on a delay relative to the excitation impulse (the excitation cycle phase) in a wide range (the maximum value exceeds the minimum by several thousand times). The results show differences in the mechanisms of impact on a cardiomyocyte between an excitation impulse and a monophasic defibrillation pulse.展开更多
文摘The behavior of the 2006 ten Tusscher-Panfilov model of human ventricular myocytes under the impact of periodic excitation impulses was studied in the BeatBox simulation environment. The cardiomyocyte model has a limited susceptibility to an forced higher frequency excitation rhythm. A high-frequency excitation rhythm can be forced by gradually increasing the frequency of excitation impulses. The mechanism of defibrillation pulse impact consists of presumably prolonging the refractoriness of cardiomyocytes which undermines their susceptibility for a long time to a forced high-frequency rhythm of fibrillation, as a result for which they hinder the propagation of a fibrillation wave. This is the only mechanism of defibrillation that was identified during the simulation. The threshold energy of a depolarizing defibrillation pulse prolonging the refractoriness of the cardio-myocyte varies depending on a delay relative to the excitation impulse (the excitation cycle phase) in a wide range (the maximum value exceeds the minimum by several thousand times). The results show differences in the mechanisms of impact on a cardiomyocyte between an excitation impulse and a monophasic defibrillation pulse.
